Sodium handling is associated with liver function impairment and renin-aldosterone axis activity in patients with preascitic cirrhosis without hyponatremia
Background In cirrhotic patients awaiting liver transplantation, serum sodium concentration
is related to prognosis. However, abnormalities in sodium homeostasis are evident even in the
early preascitic stage of cirrhosis. We aimed to investigate whether parameters of renal sodium
handling (serum sodium, urinary sodium and fractional exertion of sodium (FeNa%) correlate
with markers of liver function and renin-aldosterone axis activity in patients with preascitic
cirrhosis without hyponatremia.
Methods Patients with preascitic cirrhosis without hyponatremia underwent routine blood and
urine laboratory tests, including markers of liver function impairment and sodium homeostasis.
Results Thirty eight cirrhotic patients (22 men) with mean age of 57.3Â±12.2 (SD) years were
included. Twenty six and twelve patients were at Child-Pugh stage A and B cirrhosis respectively.
Eighteen patients had a Model for End-stage Liver Disease (MELD) score of â‰¤9 and twenty had
MELD >9. Serum sodium was found to differ significantly between Child-Pugh stage A and B
cirrhotics (mean 142.8Â±2.0 mmol/L vs. 140.5Â±3.3 mmol/L, p<0.05). Serum sodium was also
found to differ significantly between patients with MELD score â‰¤9 and >9 (mean 143.3Â±2.0
mmol/L vs. 140.9Â±2.8 mmol/L, respectively, p<0.01). Serum sodium correlated negatively with
the international normalized ratio (INR) (r=-0.51, p<0.01), aldosterone (r=-0.40, p<0.05), Child- Pugh and MELD scores (r=-0.34, p<0.05 and r=-0.45, p<0.05 respectively). FeNa% correlated negatively with renin and aldosterone (r=-0.56, p<0.001 and r=-0.50, p<0.01 respectively).
Conclusion Serum sodium concentration is a good surrogate marker of liver function impairment
not only in late-stage liver cirrhosis before transplantation but also in the early preascitic stage.
Keywords cirrhosis, liver function markers, serum sodium, Child-Pugh stage, MELD score
Ann Gastroenterol 2012; 25 (3): 254-257